Mechanisms of infective endocarditis: pathogen–host interaction and risk states

Abstract

Patients with infective endocarditis (IE) form a heterogeneous group, ranging from those who are successfully treated with no adverse events, to those with severe complications and a high mortality. In this Review, we highlight pathogen-host interactions and the mechanisms underlying various risk factors for patients with IE. A temporal trend in the pattern of IE has been observed in high-income countries within the past 5 decades, with patients contracting IE at an increasingly old age, and a growing incidence of health-care-associated staphylococcal IE. Consequently, prevention strategies should no longer focus on prophylaxis of streptococcal bacteraemia during dental procedures, but instead encourage a more-general approach to reduce the incidence of health-care-associated IE. Much knowledge has been gained about the mechanisms of vegetation formation, growth, and embolization on damaged or inflamed cardiac valves, and on cardiac devices. Improved understanding of these mechanisms will help to combat the increasing problem of antimicrobial resistance. Two mechanisms of IE should increasingly be the focus of future research: the role of immunosenescence in elderly patients with IE, particularly after transcatheter aortic valve implantation, and the mechanisms that trigger septic shock, a condition that leads to a substantial increase in the risk of death in patients with IE.

Infective Endocarditis in Elderly: From Etiology to Treatment and Prevention

“…Структурные изменения сердечных клапанов предрасполагают к агрегации тромбоцитов и колони-зации поврежденного эндотелия микроорганизмами, что приводит к развитию ИЭ [3,12]. Старческая деге-нерация клапанных структур, механическое разруше-ние эндотелия воздействуют на базовые белки вне-клеточного матрикса, стимулируют выработку ткане-вого фактора, отложение фибрина и адгезию тромбоцитов к эндотелию [13]. В преклонном возра-сте чаще регистрируются небактериальные тромбо-тические эндокардиты, которые, в свою очередь, уве-личивают вероятность развития ИЭ [14].…”

“…Эти бактерии обладают активной способностью к прикреплению и колони-зации поврежденных клапанов благодаря своим поверхностным белкам -адгезинам, способствую-щим фиксации к экстрацеллюлярным матричным белкам эндокарда [13,30].…”

Infective Endocarditis: Diagnosis, Treatment and Prevention: Review

“…7 Fibronektin, stafilokokal "clumping" faktör A ve B gibi adezyon proteinleri bakterilerin yapışmasında önemli bir role sahiptir. 7,8 Bakteri kolonizasyonu, endotel hasarını ve trombüs oluşmasını/büyüme-sini tetiklemektedir. Polisakkarit ve protein matriks içeren çok katmanlı bakteri kümeleri (agregatlar) oluşmaktadır.…”

“…İmmün yanıta göre, sepsis belirtileri genel hastalık hâlin-den şoka kadar değişmektedir. 2,6,8 Bazen hastalar, inme veya sistemik emboli gibi komplikasyon belirtileriyle başvurabilmektedir. Klinik başvuruya bakılmaksızın, açıklanamayan ısrarcı bakteremide endokardit akla getirilmeli ve araştırılmalıdır.…”

Binding of theStreptococcus gordoniiSurface Glycoprotein Hsa to α(2-3) Linked Sialic Acid Residues on Fibronectin

“…These interactions appear to be important both for the initial attachment of bacteria to the endovascular surface, and for the subsequent deposition of bacteria, immune cells, and blood components (1). However, despite the importance of these interactions in pathogenesis, a limited number of adhesins have been identified, primarily for Staphylococcus aureus.…”